Insect pheromones are crucial for survival and reproduction because they influence insect behavior, communication, and interactions within and outside the colony. Honey bees (Apis mellifera) have one of the most complex pheromonal communication systems. One pheromone, known as Queen Mandibular Pheromone (QMP), is released by the queen bee to regulate physiology, behavior, and gene expression in the female worker caste. The pheromone acts as a signal of queen presence that suppresses worker reproduction. In the absence of reproduction, young workers focus on taking care of the queen and larvae, known as nurse tasks, while older workers forage. In nurse bees, QMP has fundamental physiological impacts, including increasing abdominal lipid stores and increasing the protein content of hypopharyngeal glands (HPG). The HPG are worker-specific glands that can synthesize royal jelly used in colony nourishment. In workers, larger HPG signifies the ability to secrete royal jelly, while shrunken glands are characteristic of foragers that do not make jelly. While it is known that QMP increases abdominal lipid stores, the underlying mechanism is unclear: Does the pheromone simply make workers consume more pollen which provides lipids and protein, or does QMP also increase lipogenesis? In this study, I measured abdominal lipogenesis as fatty acid synthase (FAS) activity and monitored abdominal protein content and HPG size in caged, nurse-aged worker bees. In cages, workers were exposed to QMP or not, and they were provided with a lipid less diet in a full factorial design experiment. I found that QMP did not influence abdominal FAS activity or protein, but significantly increased HPG size. The data also revealed a significant positive correlation between abdominal protein and HPG size. My results do not support the idea that QMP modulates lipogenesis in worker bees, but my data can be interpreted to reflect that QMP mobilizes abdominal protein for the production of jelly in the HPG. This finding is in line with a previous study revealing a role of honey bee Brood Pheromone in mobilization of a major protein used in jelly production. Overall, my results support a fundamental role of QMP in worker metabolic processes associated with colony nourishment.
Maternal morbidity and mortality rates in the United States continues to rise, with a wide range of contributing factors such as mental illness, cardiovascular disease and systemic inequality. This metastudy provides a holistic view of the research that has been published on the issue of U.S. maternal healthcare from 2000-2022. The patterns of publications on specific topics over time can tell us what is perceived as a current major cause by physicians, public leaders, researchers, and the public. A deeper dive into systemic inequality as a cause of maternal morbidity and mortality highlights it as a major contributor to these high rates, but that progress is slowly being made through the implementation of detection and prevention tactics, as well as accessible prenatal programs and care.
damage, immune system activation, impaired protein function, or aberrant DNA methylation. In the case of DNA methylation, I demonstrate that inhibiting DNA methylation dynamics can impair long-term memory formation, while the nurse-to- forager transition is not altered. These experiments could serve as the bases for and reference groups of studies testing the effects of metal or metalloid toxicity on DNA methylation. Each potential mechanism provides an avenue for investigating how neural function is influenced by the physiological status of non-neural organs. And from an ecological perspective, my results highlight the need for environmental policy to consider sublethal effects in determining safe environmental toxin loads for honey bees and other insect pollinators.
Bacterial lipopolysaccharides (LPS) are structural components of the outer membranes of Gram-negative bacteria and also are potent inducers of inflammation in mammals. Higher vertebrates are extremely sensitive to LPS, but lower vertebrates, like fish, are resistant to their systemic toxic effects. However, the effects of LPS on the fish intestinal mucosa remain unknown. Edwardsiella ictaluri is a primitive member of the Enterobacteriaceae family that causes enteric septicemia in channel catfish (Ictalurus punctatus). E. ictaluri infects and colonizes deep lymphoid tissues upon oral or immersion infection. Both gut and olfactory organs are the primary sites of invasion. At the systemic level, E. ictaluri pathogenesis is relatively well characterized, but our knowledge about E. ictaluri intestinal interaction is limited. Recently, we observed that E. ictaluri oligo-polysaccharide (O-PS) LPS mutants have differential effects on the intestinal epithelia of orally inoculated catfish. Here we evaluate the effects of E. ictaluri O-PS LPS mutants by using a novel catfish intestinal loop model and compare it to the rabbit ileal loop model inoculated with Salmonella enterica serovar Typhimurium LPS. We found evident differences in rabbit ileal loop and catfish ileal loop responses to E. ictaluri and S. Typhimurium LPS. We determined that catfish respond to E. ictaluri LPS but not to S. Typhimurium LPS. We also determined that E. ictaluri inhibits cytokine production and induces disruption of the intestinal fish epithelia in an O-PS-dependent fashion. The E. ictaluri wild type and ΔwibT LPS mutant caused intestinal tissue damage and inhibited proinflammatory cytokine synthesis, in contrast to E. ictaluri Δgne and Δugd LPS mutants. We concluded that the E. ictaluri O-PS subunits play a major role during pathogenesis, since they influence the recognition of the LPS by the intestinal mucosal immune system of the catfish. The LPS structure of E. ictaluri mutants is needed to understand the mechanism of interaction.
Contemporary vaccine development relies less on empirical methods of vaccine construction, and now employs a powerful array of precise engineering strategies to construct immunogenic live vaccines. In this review, we will survey various engineering techniques used to create attenuated vaccines, with an emphasis on recent advances and insights. We will further explore the adaptation of attenuated strains to create multivalent vaccine platforms for immunization against multiple unrelated pathogens. These carrier vaccines are engineered to deliver sufficient levels of protective antigens to appropriate lymphoid inductive sites to elicit both carrier-specific and foreign antigen-specific immunity. Although many of these technologies were originally developed for use in Salmonella vaccines, application of the essential logic of these approaches will be extended to development of other enteric vaccines where possible. A central theme driving our discussion will stress that the ultimate success of an engineered vaccine rests on achieving the proper balance between attenuation and immunogenicity. Achieving this balance will avoid over-activation of inflammatory responses, which results in unacceptable reactogenicity, but will retain sufficient metabolic fitness to enable the live vaccine to reach deep tissue inductive sites and trigger protective immunity. The breadth of examples presented herein will clearly demonstrate that genetic engineering offers the potential for rapidly propelling vaccine development forward into novel applications and therapies which will significantly expand the role of vaccines in public health.
Background: Meiotic recombination has traditionally been explained based on the structural requirement to stabilize homologous chromosome pairs to ensure their proper meiotic segregation. Competing hypotheses seek to explain the emerging findings of significant heterogeneity in recombination rates within and between genomes, but intraspecific comparisons of genome-wide recombination patterns are rare. The honey bee (Apis mellifera) exhibits the highest rate of genomic recombination among multicellular animals with about five cross-over events per chromatid.
Results: Here, we present a comparative analysis of recombination rates across eight genetic linkage maps of the honey bee genome to investigate which genomic sequence features are correlated with recombination rate and with its variation across the eight data sets, ranging in average marker spacing ranging from 1 Mbp to 120 kbp. Overall, we found that GC content explained best the variation in local recombination rate along chromosomes at the analyzed 100 kbp scale. In contrast, variation among the different maps was correlated to the abundance of microsatellites and several specific tri- and tetra-nucleotides.
Conclusions: The combined evidence from eight medium-scale recombination maps of the honey bee genome suggests that recombination rate variation in this highly recombining genome might be due to the DNA configuration instead of distinct sequence motifs. However, more fine-scale analyses are needed. The empirical basis of eight differing genetic maps allowed for robust conclusions about the correlates of the local recombination rates and enabled the study of the relation between DNA features and variability in local recombination rates, which is particularly relevant in the honey bee genome with its exceptionally high recombination rate.